Suskind David L, Kong Denice, Stevens Anne, Wahbeh Ghassan, Christie Denise, Baxter-Lowe Lee-Ann, Muench Marcus O
Department of Pediatrics; Seattle Children's Hospital; University of Washington; Seattle, WA USA.
Chimerism. 2011 Apr;2(2):50-4. doi: 10.4161/chim.2.2.16556.
Inflammatory bowel disease (IBD) shares many immunologic and clinical characteristics with graft versus host disease caused by allogeneic T lymphocytes after hematopoietic cell transplantation. Since maternal cells are known to enter the fetal circulation in a high proportion of pregnancies, we hypothesized that maternal engraftment in the fetus results in immune sequelae that can lead to IBD.
The presence and extent of maternal microchimerism in tissues and blood samples from patients with Crohn's, Ulcerative colitis (UC), and control groups were determined using kinetic Polymerase Chain Reaction (kPCR) to detect maternal- and patient-specific HLA types. In addition, fluorescent in situ hybridization (FISH) was employed to detect maternal cells in biopsies from patients with IBD.
Using kPCR, maternal microchimerism was observed in 9 of the 16 (56%) patients with IBD and 6 out of 15 of the control group (40%) (P=NS). Five of 10 Crohn's patients had evidence of maternal microchimerism (50%) (P=NS). Four of six UC patients had evidence of maternal microchimerism in gut tissues (67%) (P=NS). There was no correlation between maternal michrochimerism and disease activity, disease location or granulomas in patients with IBD. Using FISH, five male Crohn's and five male UC patient's intestinal biopsies were analyzed for maternal microchimerism. No maternal cells were identified.
There is nothing in the data to suggest that patients with IBD differ from disease controls in their frequency of maternal microchimerism in either blood or gut mucosal tissues. These data suggest that maternal microchimerism in blood and biopsies is a relatively common phenomenon that has neither positive nor negative impact on IBD.
炎症性肠病（IBD）与造血细胞移植后同种异体T淋巴细胞引起的移植物抗宿主病具有许多免疫和临床特征。由于已知在大多数妊娠中母细胞会大量进入胎儿循环，我们推测母体细胞在胎儿体内植入会导致免疫后遗症，进而引发IBD。
使用动力学聚合酶链反应（kPCR）检测母体和患者特异性HLA类型，以确定克罗恩病、溃疡性结肠炎（UC）患者及对照组组织和血液样本中母体微嵌合体的存在情况及程度。此外，采用荧光原位杂交（FISH）检测IBD患者活检组织中的母体细胞。
使用kPCR，在16例IBD患者中的9例（56%）及对照组15例中的6例（40%）观察到母体微嵌合体（P=无显著性差异）。10例克罗恩病患者中有5例有母体微嵌合体证据（50%）（P=无显著性差异）。6例UC患者中有4例在肠道组织中有母体微嵌合体证据（67%）（P=无显著性差异）。IBD患者中母体微嵌合体与疾病活动、疾病部位或肉芽肿之间无相关性。使用FISH分析了5例男性克罗恩病和5例男性UC患者的肠道活检组织中的母体微嵌合体。未发现母体细胞。
数据中没有任何内容表明IBD患者在血液或肠道黏膜组织中的母体微嵌合体频率与疾病对照组有差异。这些数据表明，血液和活检组织中的母体微嵌合体是一种相对常见的现象，对IBD既无正面影响也无负面影响。
